4.7 Article

Structural Basis for Apoptosis Inhibition by Epstein-Barr Virus BHRF1

Journal

PLOS PATHOGENS
Volume 6, Issue 12, Pages -

Publisher

PUBLIC LIBRARY SCIENCE
DOI: 10.1371/journal.ppat.1001236

Keywords

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Funding

  1. Australian NHMRC [461219, 461221, 637336, 361646]
  2. NIH [CA80188, CA43540]
  3. Leukemia & Lymphoma Society (SCOR) [7413-07]
  4. Sylvia & Charles Viertel Charitable Foundation
  5. Cancer Council of Victoria
  6. Leukemia Foundation
  7. Australian Cancer Research Foundation
  8. Victorian State Government

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Epstein-Barr virus (EBV) is associated with human malignancies, especially those affecting the B cell compartment such as Burkitt lymphoma. The virally encoded homolog of the mammalian pro-survival protein Bcl-2, BHRF1 contributes to viral infectivity and lymphomagenesis. In addition to the pro-apoptotic BH3-only protein Bim, its key target in lymphoid cells, BHRF1 also binds a selective sub-set of pro-apoptotic proteins (Bid, Puma, Bak) expressed by host cells. A consequence of BHRF1 expression is marked resistance to a range of cytotoxic agents and in particular, we show that its expression renders a mouse model of Burkitt lymphoma untreatable. As current small organic antagonists of Bcl-2 do not target BHRF1, the structures of it in complex with Bim or Bak shown here will be useful to guide efforts to target BHRF1 in EBV-associated malignancies, which are usually associated with poor clinical outcomes.

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